Background

Pyridoxal isonicotinoyl hydrazone (PIH) is a tridentate Fe-chelating agent that shows high Fe chelation efficacy. In 59Fe-labeled reticulocytes, PIH (0.1 mmol/L) released 38.6% of cellular 59Fe [1]. PIH inhibited the formation of ascorbyl radical and Fe(III)–EDTA-mediated ascorbate oxidation in a dose-dependent way [3].

In Fe-loaded rats, PIH orally administrated resulted in an eightfold increase in fecal Fe excretion and possibly some urinary excretion of Fe [1]. In mice loaded with iron-acetohydroxamic acid complex, pyridoxal isonicotinoyl hydrazone (po.) were given daily for four days at 300 mg/kg/day. Total iron excreted over the 4-day period (micrograms/mouse) was 31 [2]. Pyridoxal isonicotinoyl hydrazine could be used for experimental chelating therapy in iron-overload diseases [3].